K
Keigo Machida
Researcher at University of Southern California
Publications - 92
Citations - 5098
Keigo Machida is an academic researcher from University of Southern California. The author has contributed to research in topics: Homeobox protein NANOG & Hepatitis C virus. The author has an hindex of 37, co-authored 78 publications receiving 4422 citations. Previous affiliations of Keigo Machida include University of Tsukuba & Sapporo Medical University.
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Journal ArticleDOI
Hepatitis C virus induces a mutator phenotype: Enhanced mutations of immunoglobulin and protooncogenes
Keigo Machida,Kevin T.-N. Cheng,Vicky M.-H. Sung,Shigetaka Shimodaira,Karen L. Lindsay,Alexandra M. Levine,Ming-Yang Lai,Michael M. C. Lai +7 more
TL;DR: It is demonstrated that acute and chronic HCV infection caused a 5- to 10-fold increase in mutation frequency in Ig heavy chain, BCL-6, p53, and β-catenin genes of in vitro HCV-infected B cell lines andHCV-associated peripheral blood mononuclear cells, lymphomas, and HCCs.
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NANOG Metabolically Reprograms Tumor-Initiating Stem-like Cells through Tumorigenic Changes in Oxidative Phosphorylation and Fatty Acid Metabolism
Chia-Lin Chen,Dinesh Babu Uthaya Kumar,Vasu Punj,Jun Xu,Linda Sher,Stanley M. Tahara,Sonja Hess,Keigo Machida +7 more
TL;DR: It is shown that NANOG is induced by Toll-like receptor 4 (TLR4) signaling via phosphorylation of E2F1 and that downregulation of Nanog slows down hepatocellular carcinoma (HCC) progression induced by alcohol western diet and hepatitis C virus protein in mice.
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Hepatitis C Virus Triggers Mitochondrial Permeability Transition with Production of Reactive Oxygen Species, Leading to DNA Damage and STAT3 Activation
Keigo Machida,Kevin T.-H. Cheng,Chao-Kuen Lai,King-Song Jeng,Vicky M.-H. Sung,Michael M. C. Lai,Michael M. C. Lai +6 more
TL;DR: It is reported that HCV infection causes production of reactive oxygen species (ROS) and lowering of mitochondrial transmembrane potential (ΔΨm) in in vitro HCV-infected cell cultures, and ROS, along with the previously identified NO, are identified as the primary inducers of DSBs and mitochondrial damage in HCV -infected cells.
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Toll-like receptor 4 mediates synergism between alcohol and HCV in hepatic oncogenesis involving stem cell marker Nanog
Keigo Machida,Hidekazu Tsukamoto,Hasmik Mkrtchyan,Lewei Duan,Alla Dynnyk,Helene Minyi Liu,Kinji Asahina,Sugantha Govindarajan,Ratna B. Ray,Jing-hsiung James Ou,Ekihiro Seki,Raymond J. Deshaies,Kensuke Miyake,Michael M. C. Lai +13 more
TL;DR: This study provides the first evidence that Toll-like receptor 4 (TLR4) is induced by hepatocyte-specific transgenic expression of the HCV nonstructural protein NS5A, and this induction mediates synergistic liver damage and tumor formation by alcohol-induced endotoxemia.
Journal ArticleDOI
Hepatitis C Virus Induces Toll-Like Receptor 4 Expression, Leading to Enhanced Production of Beta Interferon and Interleukin-6
Keigo Machida,Kevin T.-H. Cheng,Vicky M.-H. Sung,Alexandra M. Levine,Steven K. H. Foung,Michael M. C. Lai +5 more
TL;DR: Hepatitis C virus infection directly induces TLR4 expression and thereby activates B cells, which may contribute to the host's innate immune responses, and this study analyzes expression and regulation in human B cells following HCV infection in vitro.